The role of TGF-β in polycystic ovary syndrome

Nazia Raja-Khan; Margrit Urbanek; Raymond J. Rodgers; Richard S. Legro

doi:10.1177/1933719113485294

The role of TGF-β in polycystic ovary syndrome

Nazia Raja-Khan^*, Margrit Urbanek, Raymond J. Rodgers, Richard S. Legro

^*Corresponding author for this work

Medicine, Endocrinology Division

Research output: Contribution to journal › Review article › peer-review

97 Scopus citations

Abstract

Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by chronic oligoanovulation and hyperandrogenism and associated with insulin resistance, type 2 diabetes, and cardiovascular risk. In recent years, genetic studies have linked PCOS to a dinucleotide marker D19S884 in the fibrillin 3 gene. Fibrillins make up the major component of microfibrils in the extracellular matrix (ECM) and interact with molecules in the ECM to regulate transforming growth factor β (TGF-β) signaling. Therefore, variations in fibrillin 3 and subsequent dysregulation of TGF-β may contribute to the pathogenesis of PCOS. Here, we review the evidence from genetic studies supporting the role of TGF-β in PCOS and describe how TGF-β dysregulation may contribute to (1) the fetal origins of PCOS, (2) reproductive abnormalities in PCOS, and (3) cardiovascular and metabolic abnormalities in PCOS.

Original language	English (US)
Pages (from-to)	20-31
Number of pages	12
Journal	Reproductive Sciences
Volume	21
Issue number	1
DOIs	https://doi.org/10.1177/1933719113485294
State	Published - Jan 2014

Keywords

TGF-β
fetal origins
fibrillin
genetics
polycystic ovary syndrome

ASJC Scopus subject areas

Obstetrics and Gynecology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1177/1933719113485294

Cite this

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title = "The role of TGF-β in polycystic ovary syndrome",

abstract = "Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by chronic oligoanovulation and hyperandrogenism and associated with insulin resistance, type 2 diabetes, and cardiovascular risk. In recent years, genetic studies have linked PCOS to a dinucleotide marker D19S884 in the fibrillin 3 gene. Fibrillins make up the major component of microfibrils in the extracellular matrix (ECM) and interact with molecules in the ECM to regulate transforming growth factor β (TGF-β) signaling. Therefore, variations in fibrillin 3 and subsequent dysregulation of TGF-β may contribute to the pathogenesis of PCOS. Here, we review the evidence from genetic studies supporting the role of TGF-β in PCOS and describe how TGF-β dysregulation may contribute to (1) the fetal origins of PCOS, (2) reproductive abnormalities in PCOS, and (3) cardiovascular and metabolic abnormalities in PCOS.",

keywords = "TGF-β, fetal origins, fibrillin, genetics, polycystic ovary syndrome",

author = "Nazia Raja-Khan and Margrit Urbanek and Rodgers, {Raymond J.} and Legro, {Richard S.}",

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AU - Raja-Khan, Nazia

AU - Urbanek, Margrit

AU - Rodgers, Raymond J.

AU - Legro, Richard S.

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Y1 - 2014/1

N2 - Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by chronic oligoanovulation and hyperandrogenism and associated with insulin resistance, type 2 diabetes, and cardiovascular risk. In recent years, genetic studies have linked PCOS to a dinucleotide marker D19S884 in the fibrillin 3 gene. Fibrillins make up the major component of microfibrils in the extracellular matrix (ECM) and interact with molecules in the ECM to regulate transforming growth factor β (TGF-β) signaling. Therefore, variations in fibrillin 3 and subsequent dysregulation of TGF-β may contribute to the pathogenesis of PCOS. Here, we review the evidence from genetic studies supporting the role of TGF-β in PCOS and describe how TGF-β dysregulation may contribute to (1) the fetal origins of PCOS, (2) reproductive abnormalities in PCOS, and (3) cardiovascular and metabolic abnormalities in PCOS.

AB - Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by chronic oligoanovulation and hyperandrogenism and associated with insulin resistance, type 2 diabetes, and cardiovascular risk. In recent years, genetic studies have linked PCOS to a dinucleotide marker D19S884 in the fibrillin 3 gene. Fibrillins make up the major component of microfibrils in the extracellular matrix (ECM) and interact with molecules in the ECM to regulate transforming growth factor β (TGF-β) signaling. Therefore, variations in fibrillin 3 and subsequent dysregulation of TGF-β may contribute to the pathogenesis of PCOS. Here, we review the evidence from genetic studies supporting the role of TGF-β in PCOS and describe how TGF-β dysregulation may contribute to (1) the fetal origins of PCOS, (2) reproductive abnormalities in PCOS, and (3) cardiovascular and metabolic abnormalities in PCOS.

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The role of TGF-β in polycystic ovary syndrome

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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